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By V. Rune. Notre Dame de Namur University.

Reproducible initiation of counterclockwise flutter is possible in more than 95% of patients if a protocol including introduction of up to two extrastimuli at multiple drive cycle lengths (600 to 300 msec) buy finast canada, at multiple atrial sites finast 5mg discount, and rapid pacing to 180 msec is completed order finast cheap online. Those patients with clockwise, isthmus-dependent flutter also have a high likelihood of inducibility. The reason for this early fractionation and period of what appears to be atrial fibrillation or impure atrial flutter may be the instability prior to formation of a line of block along the tendon of Todero and/or the Eustachian ridge. B: In the bottom panel the atrial activation pattern is disorganized, consistent with atrial fibrillation. Hybrid pharmacologic and ablative therapy: a novel and effective approach for the management of atrial fibrillation. While the overall frequency of any single extrastimulus or two extrastimuli initiating atrial flutter is low (less than 10%), the ability to initiate atrial flutter in any individual with a prior history of atrial flutter exceeds 90%. In our experience at the University of Pennsylvania atrial flutter was inducible in the laboratory by programmed stimulation using either one P. A similar incidence of inducibility of atrial flutter was found in 524 consecutive patients with a prior history of that arrhythmia studied at the Beth Israel Deaconess Medical Center from 1994 to 2011. The inducibility rate was 95% in patients who ultimately were proven to have isthmus-dependent flutter. Of note, the more rapid atrial pacing that is performed and the closer coupled atrial extrastimuli are delivered, the more likely atrial fibrillation (usually self-terminating) is induced, though the incidence of sustained atrial fibrillation is less than 10%. The significance of induction of atrial fibrillation in these patients is uncertain. Thus, failure to induce atrial flutter is rare in patients who have a history of atrial flutter as long as a complete stimulation protocol is employed. However, because of the induction of atrial fibrillation, in some patients atrial flutter may not be inducible. A single atrial premature1 depolarization (S ) delivered at a coupling interval of 170 msec during a basic drive cycle length (S -S ) of 6002 1 1 msec induces atrial flutter. Its induction in a patient without a prior history of atrial flutter or fibrillation is extremely rare. It is of interest that when counterclockwise and clockwise flutter are induced in the same patient, the cycle lengths are similar, although in our experience the cycle lengths of counterclockwise flutter may occasionally be slightly shorter. Differences in cycle length must be related to anisotropy and/or differences in electrophysiologic properties within the circuit, which are activated at different points in time during initiation and maintenance of flutter. Such delays in fragmentation are also seen in patients who develop atrial fibrillation (see section on activation mapping and programmed stimulation, page 300 and Fig. It is of note that when rapid atrial pacing is used to initiate the arrhythmia, the efficacy of inducibility from both sites is comparable. Decremental conduction, which has been demonstrated in the isthmus, may be critical when rapid atrial pacing is used to initiate atrial flutter, while nonuniform anisotropy may be more important during single and double extrastimuli. Further investigation of these concepts is necessary to clarify the role of nonuniform anisotropy, dispersion of refractoriness, and abnormalities of propagation in the isthmus in initiation of atrial flutter during different stimulation techniques. Regardless of mechanism, the site of block required for initiation of flutter appears to be in the isthmus (Figs. Initial paced beats show simultaneous counterclockwise and clockwise activation of the right atrium (see arrows on second beat). Mechanism of initiation of atrial flutter in humans: site of unidirectional block and direction of rotation. This transient appearance of what could be considered local atrial fibrillation may in fact reflect the setting up of lines of block that form the barriers necessary 63 to define the flutter circuit. While the isthmus is the site of block regardless of whether or not clockwise or counterclockwise flutter is 63 induced, the direction of rotation may be dependent on the site of stimulation. We did note, however, that clockwise flutter was almost always induced from the anterolateral right atrium or right 63 atrial appendage, which is in full accordance with Olgin et al. One of the reasons for differences is their exclusion of patients with irregular atrial rhythms in transition to stable 63 atrial flutter. Of interest is the fact that atrial flutter induced in transplanted hearts always has a counterclockwise rotation regardless of the site of stimulation 24 and the absence of any role of the crista terminalis. Thus, it is misleading for electrophysiologists to think that flutter is difficult to induce. One needs to use relatively short coupled atrial extrastimuli at shorter-paced cycle lengths or rapid atrial pacing to induce the rhythm. If the late coupled atrial premature complexes and the “slow” rates of rapid atrial pacing are excluded, the chance of initiating flutter is high. Certainly it is reproducible and, in my opinion, is a reasonable, albeit not perfect, end point for judging the therapeutic efficacy of pharmacologic or ablative interventions. On the third beat block in the isthmus occurs leading to initiation of clockwise flutter. Mechanism of initiation of atrial flutter in humans: site of unidirectional block and direction of rotation. This may be particularly true in flutters that arise in the left atrium or are associated with prior surgical interventions. Activation Mapping and Programmed Stimulation During Flutter Characterization of the reentrant circuit in isthmus-dependent flutter has evolved over the past decade. This has been a result of more detailed mapping of the right atrium and sometimes the left atrium during flutter, in combination with programmed stimulation. In addition, the recent use of the Carto system (Biosense, Cordis Webster; Johnson and Johnson; see Chapter 2) has allowed acquisition of several hundred sequentially mapped sites that are then plotted as both an isochronic activation map and a propagation map. Both mapping presentations clarify the reentrant circuit used for isthmus-dependent clockwise and counterclockwise flutters (Fig. Use of this system has also been valuable in analyzing atypical flutters arising from the left atrium or prior surgical incisions (Fig. Noncontact mapping (Navix, St Jude Medical) and the use of multipolar basket catheters also have great potential for furthering our knowledge of different atrial flutters. The most important catheters for characterizing isthmus-dependent flutters have been the use of multipolar standard or deflectable catheters with 10 to 20 poles. Depending on the catheter used, the proximal poles may actually record from the septum and the middle poles the anterior right atrium.

Adipose tissue and lipid droplet embolism following periurethral injection of autologous fat: Case report and review of the literature finast 5 mg cheap. Complications of sterile abscess formation and pulmonary embolism following periurethral bulking agents order finast 5 mg overnight delivery. Cystoscopic injections of dextranomer hyaluronic acid into proximal urethra for urethral incompetence: Efficacy and adverse outcomes generic finast 5mg on line. Use of ethylene vinyl alcohol copolymer for tubal sterilization by selective catheterization in rabbits. The safety and efficacy of ethylene vinyl alcohol copolymer as an intra-urethral bulking agent in women with intrinsic urethral deficiency. Polytef (Teflon) migration after periurethral injection: Tracer and x- ray microanalysis techniques in experimental study. Delivery of injectable agents for treatment of stress urinary incontinence in women: Evolving techniques. Antegrade techniques of collagen injection for post-prostatectomy stress urinary incontinence: The Washington University experience. A multicentre evaluation of a new surgical technique for urethral bulking in the treatment of genuine stress incontinence. Results of transurethral injection of silicone micro-implants for females with intrinsic sphincter deficiency. Bulking agents for stress urinary incontinence: Short-term results and complications in a randomized comparison of periurethral and transurethral injections. Comparison of transurethral versus periurethral collagen injection in women with intrinsic sphincter deficiency. Transurethral implantation of macroplastique for the treatment of female stress urinary incontinence secondary to urethral sphincter deficiency. New periurethral bulking agent for stress urinary incontinence: Modified technique and early results. Evaluation of the poly-L-lactic acid implant for treatment of the nasolabial fold: 3-year follow-up evaluation. Simple aspiration technique to address voiding dysfunction associated with transurethral injection of dextranomer/hyaluronic acid copolymer. Massive prolapse of the urethral mucosa following periurethral injection of calcium hydroxylapatite for stress urinary incontinence. Large urethral prolapse formation after calcium hydroxylapatite (Coaptite) injection. Delayed presentation of pseudoabscess secondary to injection of pyrolytic carbon-coated 784 beads bulking agent. Periurethral abscess following polyacrylamide hydrogel (Bulkamid) for stress urinary incontinence. Abscess formation and local necrosis after treatment with Zyderm or Zyplast collagen implant. Periurethral mass formations following bulking agent injection for the treatment of urinary incontinence. Particle migration after transurethral injection of carbon coated beads for stress urinary incontinence. New onset vesicovaginal fistula after transurethral collagen injection in women who underwent cystectomy and orthotopic neobladder creation: Presentation and definitive treatment. Three-dimensional ultrasonography: An objective outcome tool to assess collagen distribution in women with stress urinary incontinence. Role of three-dimensional ultrasound in assessment of women undergoing urethral bulking agent therapy. Urethral bulking with polymethylmethacrylate microspheres for stress urinary incontinence: Tissue persistence and safety studies in miniswine. Directed in vitro myogenesis of human embryonic stem cells and their in vivo engraftment. Autologous muscle derived cell therapy for stress urinary incontinence: A prospective, dose ranging study. Clonal isolation of muscle-derived cells capable of enhancing muscle regeneration and bone healing. Autologous muscle-derived cells for the treatment of female stress urinary incontinence: A 2-year follow-up of a Polish investigation. Over time, its use has expanded for the treatment of a variety of multiple conditions, including migraine headaches, limb spasticity, cosmetic surgery, muscular dystonia, and lower urinary tract dysfunction [1]. Biology and Mechanism of Action Clostridium botulinum is a Gram-positive anaerobic bacterium, whose strains produce seven immunologically distinct neurotoxins (types A–G). Types A and B have been used to treat medical conditions, with type A being used most often as it is relatively easily obtained and stable. The neurotoxin component is synthesized as a biologically inactive single-chain polypeptide activated by cleavage of the polypeptide chain into a 100-kDa heavy chain and a 50-kDa light chain linked by a disulfide bond [8,9]. There are a variety of type A botulinum toxin products available; these products are not equivalent and the doses are not interchangeable. Under normal circumstances in striated muscle, each muscle fiber is innervated by a single motor neuron at a site near the middle of each muscle fiber. Within each nerve terminal are cystoplasmic vesicles containing Ach transmitter molecules. The Ach collects within clusters of these synaptic vesicles and each vesicle aligns with a patch of dense material forming an active zone. At the active zone in response to a propagated neural impulse, vesicles fuse with the plasma membrane resulting in the release of the Ach transmitter molecules into the synaptic cleft. The Ach diffuses across the synaptic cleft, binding to and stimulating the postsynaptic Ach receptors on the muscle cell. Its heavy chain is involved in the binding of the neurotoxin and in the transportation of the neurotoxin into the neuronal cytosol (endocytosis). Without the release of Ach into the synaptic cleft, there is no muscle contraction. Additionally, many patients continue to experience urinary leakage despite maximum medical therapy. In such patients, initiation of intermittent catheterization is necessary to effect bladder emptying. Incontinence was resolved in 17 of 19 patients and the clinical effect was still present at 9 months in the 11 patients who were still being followed [3].

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Anatomically contoured implants of adequate size and shape present very few problems in malposition or mobil- 16 Technical Elements ity because they fill the space comfortably and hold their position by virtue of their contoured posterior surface and The various routes for entering the malar space order finast 5mg overnight delivery, including their rapid fixation to bone buy generic finast pills. Minimize bleeding by using both local and general anes- blepharoplasty (subcilial) finast 5mg cheap, (3) rhytidectomv, (4) zygomatico- thesia. A “dry operative field” is essential for accurate temporal, (5) transcoronal, and (6) transconjunctival. The visualization, precise dissection, and proper placement, intraoral route has been the traditional and most frequent the three critical factors in avoiding potential problems approach to maxillary malar and midface augmentation. The with hematoma, seroma, infection, inaccurate placement, authors use an incision that is L shaped with 1 cm limbs, and nerve damage. Maintenance of the systolic blood made through the mucosa only and in a vertically oblique pressure between 90 and 110 provides optimal hemosta- direction. It is located over the anterior buttress of the max- sis in combination with infiltration of a dilute lidocaine illa, just above the canine tooth and approximately 2. Terino mobilized, both lateral and inferior to the infraorbital fora- men, with a careful scraping motion until the nerve and fora- men is visualized. This is indicated for placement of Lower aesthetic suborbital tear trough implants. Frequent irrigation is per- unit formed with antibiotic solution (Bacitracin, 50,000 U/L or Ancef 1 g/L of normal saline). Once the space is mobilized, the chosen implant is intro- duced with a long, curved, serrated clamp placed transversely across the upper end of the implant and inserted into the pos- Submandibular implant lengthens the face in the vertical dimension terior zygomatic tunnel while two 10-in. Should buckling of the implant occur, correct positioning can be ensured by using a Russian forceps, in combination with a spatula periosteal elevator, passed both anterior and posterior to the implant. Fiberoptic Aufricht retractors or other illuminating instruments are used to illu- minate the interior of the space, reveal the internal anatomy and confirm the correct position of the implant. In the submalar zone, the soft tissues are swept off the shiny, white, glistening, fibrous tendon of the masseter mus- cle in an inferior and outward direction. This opens up the submalar space for approximately 1–2 cm, depending on the desired choice of cheek shape and the corresponding implant necessary to achieve it. When adequate anesthesia tech- niques are used, the intraoral approach permits excellent Fig. It permits the surgeon to place a spatula eleva- tor above and below the implant to make certain that its A spatula-shaped elevator with a 1-cm wide blade is edges are not buckled or that the zygomatic extension of the thrust directly under the periosteum and under the orbicu- implant is not curled. It is not necessary to visualize the laris oris muscle in a vertical orientation at the inferior base infraorbital nerve, but it is rather easy to do so when required, of the maxillary buttress, in the apex of the gingival buccal or when an implant is used for the suborbital region. The overlying soft tissues are swept obliquely upward over the maxillary eminence by maintaining the elevator directly on bone. The elevator should always remain on the 17 Subciliary Blepharoplasty Approach bony margin along the inferior border of the malar eminence and zygomatic arch (Fig. In the standard subciliary blepharoplasty approach, an inci- Manual palpation of the previously marked zonal design sion is made 3 mm below the lash line, and limited in its of the malar space anatomy on the skin is performed, while lateral extension to avoid scars in the lateral canthal region. This maneuver includes palpating the orbital rim tine blepharoplasty or as an independent route of entry for a and the upper and lower borders of the zygoma as the eleva- malar implant. When used for implant placement alone, the tor dissects the subperiosteal space within these areas incision is limited to a length of 10–15 mm. Once bony margins are reached, further provides a sturdy shelf upon which the implant rests. No dissection should occur into the subcilial blepharoplasty incision, a transconjunctival inci- soft tissues with a penetrating and forceful motion. The tear trough implant is placed No dissection should occur directly into the area of the after cutting out a segment, which allows it to surround the infraorbital nerve. If desired, it can be 3D Facial Volumization with Anatomic Alloplastic Implants 1019 Fig. Top and bottom: before rhinoplasty, central chin and angle of jaw implants 3D Facial Volumization with Anatomic Alloplastic Implants 1021 secured by one or two sutures to the medial orbicularis mus- 18 Premandible Augmentation cles or to the inferior orbital rim. Technique The greatest advantage of the subcilial blepharoplasty approach is the opportunity for correct positioning, because E xtending a centrally placed implant into the midlateral and the surgeon is able to directly observe the relationship of the posterolateral zones requires only a dissection along the implant to the inferior orbital rim. There is a significant constriction and Table 1 I deal qualities for facial implants adherence of the tissues to the bone surrounding the mental Silicone Gore-Tex/ Porex/ foramen called the mandibular ligament. Once these are I deal Qualities Rubber Soft Form Medpor Hydroxyapatite released, dissection of the tissues from the posterolateral Biocompatible 4 3 4 4 zone occurs easily. Modifiable 4 2 3 3 Although operations to augment the central mandible for E xchangeable 4 2 1 1 aesthetic purposes have existed for over 50 years (Millard Resistant to 3 1 3 2 1953) [16], and plastic surgeons have well understood the Infection advantages of improved nasomentum profile relationships, it Anatomic contours 4 1 2 2 is only within the last 30 years that methods have been devel- Visible, palpable 3. These techniques Table 2 I deal anesthesia for alloplastic facial contouring also make it possible to alter the shape and size of the mid- lateral and posterior aspects of the mandible, and even to General anesthesia Maintain blood pressure at 90–100 systolic lengthen the submandibular segment vertically. Clonidine, 2 mg orally preoperatively A ccess to the premandible space can be achieved by Local anesthesia either the standard intraoral route or the submental route Lidocaine solution 0. These authors use the submental approach exclu- A drenalin 1:800,000 sively for operations that require additional surgery in the Generous tissue infiltration into malar or premandible space submental and submandibular region, such as liposculptur- (20–30 ml each) ing and platysmal contouring "L" extension Incision Sulcus Fig. B y adhering to the principle of subperiosteal elevation on bone, the muscle attachments are elevated from their origins along the inferior margin of the mandible. Consequently, it is important not to traumatize the tissues that overlie and constitute the roof of the premandible space in that region. The bony configuration of the foramen, however, directs the mental nerve in a superior path upward into the lower lip. Dissections that remain inferior to the foramen and along the lower border of the mandible avoid significant danger of nerve damage. In one operation, the senior author inadvertently placed a premandible implant superior to the mental nerves bilater- ally. The immediate result was compression symptoms in the form of anesthesia of the lower lip. Replacement of an In both approaches, the incisions are transverse and 2 cm implant or repositioning can easily be done within the first long. The mentalis muscles are then divided vertically ing taught during residency, the surgeon is able to reenter the through their midline raphe to avoid transection of the mus- premandible or malar space to replace or reposition implants cle bellies and total detachment from their bony origins prior to the rapid increase in wound tensile strength, which (Fig. This aperture provides direct access downward occurs from 14 to 21 days after the operation. A dditional incisions may be made posterior to the mental nerve to accurately place lateral mandibular bars and implants that extend into the midlateral and posterolateral zones. A 3-cm horizontal mucosal incision made in front of the first molar, followed by direct penetration through the b muscle onto the mandibular bone, allows access to, and easy dissection of, the premandible space beneath. This aperture assists accurate placement of mandibular angle implant and also facilitates positioning the posterior extensions of other implants to augment simultaneously the central mentum and the midlateral zones anteriorly.

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The commonly used time scale is 5 or 10 ms/division cheap finast 5mg on-line, with an amplitude gain of 50–500 μV/division (Figure 36 cheap finast online american express. Amplitude is highly sensitive to needle position and very minor adjustments of the electrode will result in major changes order finast 5 mg online, i. The duration of a motor unit is the time between the first deflection and the point when the waveform finally returns to the baseline. This will depend on the number of muscle fibers within the motor unit and is little affected by the proximity of the recording electrode to the nearest fiber. The difficulty with this measurement is defining the exact point of return to the baseline. A related parameter is a “turn,” which is defined as a shift in direction of a potential of greater than a specified amplitude. At this detection site, three motor unit potentials are firing continuously and can be analyzed. The technical differences in the methods are many and no in-depth description is attempted here. This makes quantitative analysis much simpler and results from different laboratories easily comparable. Similar in-depth analyzed normative data from standardized techniques for other pelvic floor and perineal muscles are not yet available, but individual laboratories use their own normative data. The original recording needles are specially constructed (with a small recording area oriented “sideways” on the thin cannula; Figure 36. Thus, the contribution of each muscle fiber appears as a biphasic positive–negative action potential. Small changes with age have been reported; women have significantly greater fiber density than men [28]. Between 10 and 20 days after a denervating injury, “insertion activity” becomes more prolonged and abnormal spontaneous activity in the form of short biphasic spikes (“fibrillation potentials”) and biphasic potentials with prominent positive deflections (“positive sharp waves”) appear [38]. In perineal muscles, complete denervation can be observed after traumatic lesions to the lumbosacral spine and damage to the cauda equina. In long-standing partially denervated muscle, a peculiar abnormal insertion activity appears, the so-called repetitive discharges. These are made up of repetitively firing groups of potentials with so little jitter between the potentials that it is assumed the activity must be due to ephaptic or direct transmission of impulses between muscle fibers [30]. However, this activity may be found in the striated muscle of the urethral sphincter without any other evidence of neuromuscular disease and it has been hypothesized that it causes impaired relaxation of the muscle when spontaneous and profuse [31]. In partially denervated muscle, collateral reinnervation takes place; surviving motor axons will sprout and grow out to reinnervate those muscle fibers that have lost their nerve supply, resulting in a change in the arrangement of muscle fibers within the unit. Whereas in healthy muscle, it is unusual for two adjacent muscle fibers to be part of the same motor unit, following reinnervation several muscle fibers all belonging to the same motor unit come to be adjacent to one another. Early in the process of reinnervation, the newly outgrown motor sprouts are thin and therefore conduct slowly so that the time taken for excitatory impulses to spread through the axonal tree is abnormally prolonged. Neuromuscular transmission in these newly grown 529 sprouts may also be insecure so that the motor unit may show “instability. This phenomenon may be different in the sphincter muscles where long duration motor units seem to remain a prominent feature of reinnervated motor units [33]. There are several conditions in which gross changes of reinnervation may be detected in motor units of the pelvic floor. Autonomic failure causing postural hypotension and cerebellar ataxia causing unsteadiness and clumsiness may be additional features. Urinary incontinence in both women and men occurs early in this condition, often appearing some years before the onset of obvious neurological features, and not uncommonly, patients may present to the urologist [36]. As part of the neurodegenerative process, selective loss of anterior horn cells occurs in Onuf’s nucleus so that partial but progressive denervation of the sphincter occurs and recorded motor units show changes of reinnervation, becoming markedly prolonged. Studies using computer-assisted quantified and less operator-biased techniques have confirmed older findings [43,44] of at least subtle neurogenic pelvic floor muscle changes in parous women [25,45]. The abnormalities demonstrated in external anal sphincter and pudendal nerves have been suggested to be of pathogenetic significance and also for idiopathic fecal incontinence [47]. The development of imaging techniques has improved the diagnosis of postpartum structural (anatomical) damage to pelvic floor structures (including sphincters), which has put the importance of the postpartum neurogenic electrophysiological changes in perspective, which, when minor, may have little functional consequences. The neurogenic damage caused by vaginal delivery is acknowledged to be, to a large extent, repaired by regenerative processes, but may then recur in the long run [47]. Repetitive straining at stool due to constipation has been the main implicated pathogenetic mechanism for such chronic progression of the neuromuscular lesion. Indeed, prolongation of pudendal nerve terminal latency has been demonstrated after 1 minute of hard straining [48]. Cumulative damage to the pudendal nerve may occur in severe chronic constipation; our study in patients with mild chronic constipation failed, however, to reveal any neurogenic anal sphincter changes, as compared to nonconstipated controls [27]. On the other hand, myogenic changes in pelvic floor muscles after vaginal delivery were also reported [49]. It was proposed that this pathological spontaneous activity leads to sphincter contraction, which endures during micturition and causes obstruction to flow. The syndrome described by Clare Fowler is associated with polycystic ovaries (Fowler’s syndrome) [51]. Sustained contraction of the urethral sphincter has an inhibitory effect on bladder afferents and efferents, resulting in loss of bladder sensation and urinary retention. The mean age of a series of women with this problem was 27 years; spontaneous onset appears to be more common in women under 30 [52]. Characteristically, the women present with a bladder capacity in excess of 1 L, and, although this may cause painful distension, they lack any expected sensations of urinary urgency. There may or may not be a history of infrequent voiding prior to the onset of urinary retention. These women are taught to do clean intermittent self-catheterization and commonly experience difficulties with this technique, in particular pain and difficulty in removing the catheter. It should certainly be carried out before stigmatizing a woman as having “psychogenic urinary retention.

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